ENDOTOXIN INTERACTS WITH TUMOR NECROSIS FACTOR-α TO INDUCE VASODILATION OF ISOLATED RAT SKELETAL MUSCLE ARTERIOLES

Glembot, Troy M.; Britt, L. D.; Hill, Michael A.

doi:10.1097/00024382-199604000-00004

Cited by 24 publications

(19 citation statements)

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“…2, C-F). In contrast, studies have shown that TNF-␣ alters vascular contractile responses (8,23,30,31,35). This ostensible discrepancy may be due to the difference in used blood vessels.…”

Section: Discussionmentioning

confidence: 95%

“…Since both RhoA/Rho-kinase (29) and TNF-␣ (8,23,30,31,35) are implicated in the genesis of vascular dysfunction, it is also likely that a TNF-␣/RhoA/Rho-kinase pathway in vascular smooth muscle cells may be pathophysiologically important. Our study, although providing important new findings, has some limitations.…”

Section: Discussionmentioning

confidence: 99%

“…However, there are some inconsistent results. For example, TNF-␣ in rat skeletal muscle arterioles does not have any direct vasoconstrictor effect and exerts a vasodilator action in the presence of endotoxin (8).…”

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confidence: 99%

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Dual regulation of tumor necrosis factor-α on myosin light chain phosphorylation in vascular smooth muscle

Chen

Hall

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

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We previously demonstrated that inhibitor κB kinase 2 (IKK2) is a myosin light chain kinase (MLCK). In the present study, we assess whether the prototypical activator of IKK2 tumor necrosis factor-α (TNF-α) regulates the MLCK activity of IKK2 and thus MLC phosphorylation in vascular smooth muscle cells (VSMCs). Kinase activity assay revealed that TNF-α downregulated the MLCK activity of IKK2 in human VSMCs (HVSMCs). However, Western blot analysis did not demonstrate a significant effect of TNF-α on MLC phosphorylation in HVSMCs, and myograph analysis did not reveal a significant effect of TNF-α on the contraction of the aorta from Sprague-Dawley rats and C57Bl/6j mice, suggesting a dual regulation of MLC phosphorylation by TNF-α. Confirming this notion, TNF-α significantly increased MLC phosphorylation in IKK2−/− but not wild-type cells. Furthermore, our results show that TNF-α increased GTP-bound RhoA and MLC phosphatase subunit MYPT1 phosphorylation and markedly reduced MLC phosphorylation in the presence of Rho-kinase inhibitor Y-27632, suggesting that downregulation of MLCK activity of IKK2 by TNF-α is antagonized by simultaneous RhoA/Rho-kinase activation. These results indicate that TNF-α dually regulates MLC phosphorylation through both IKK2 and RhoA/Rho-kinase pathways.

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Section: Discussionmentioning

confidence: 95%

Section: Discussionmentioning

confidence: 99%

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Dual regulation of tumor necrosis factor-α on myosin light chain phosphorylation in vascular smooth muscle

Chen

Hall

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

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“…However, the exact mechanism of this cytokine is still somewhat controversial. For example, in the cochlear microvasculature, it has been reported to increase vascular tone [31], whereas in skeletal muscle arterioles, it seems to induce vasodilation [32]. Furthermore, in pregnant but not in female control rats, TNFα was able to induce an increase in blood pressure [33], which strongly indicates a context dependent effect of the cytokine.…”

Section: Discussionmentioning

confidence: 99%

Increased Contractile Response to Noradrenaline Induced By Factors Associated with the Metabolic Syndrome in Cultured Small Mesenteric Arteries

Blædel

Sams²,

Boonen³

et al. 2015

Pharmacology

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This study investigated the effect of the metabolic syndrome associated risk factors hyperglycemia (glucose [Glc]), hyperinsulinemia (insulin [Ins]) and low-grade inflammation (tumor necrosis factor α [TNFα]) on the vasomotor responses of resistance arteries. Isolated small mesenteric arteries from 3-month-old Sprague-Dawley rats, were suspended for 21-23 h in tissue cultures containing either elevated Glc (30 mmol/l), Ins (100 nmol/l), TNFα (100 ng/ml) or combinations thereof. After incubation, the vascular response to noradrenaline (NA), phenylephrine, isoprenaline and NA in the presence of propranolol (10 µmol/l) was measured by wire myography. Results: Arteries exposed only to combinations of the risk factors showed a significant 1.6-fold increase in the contractile NA sensitivity, which suggests that complex combinations of metabolic risk factors might lead to changes in vascular tone.

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“…Multiple mediators released during sepsis such as nitric oxide (NO), tumor necrosis factor-␣, and different interleukins have been implicated in the events leading to a decrease in vascular resistance. Previous research in this laboratory has shown that these agents are capable of inhibiting vascular tone in vivo but when endotoxin was exposed to a single isolated rat cremasteric arteriole, no loss of tone was noted [1,2]. However, when a segment of rat aorta was placed upstream and in series to the isolated arteriole, endotoxin exposure produced significant vasodilatation [3].…”

Section: Introductionmentioning

confidence: 95%

Endotoxin releases a precursor to vasodilation from large veins in an NF-κB-dependent manner

Campsen

Snyder

Prewitt

et al. 2004

Journal of Surgical Research

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ENDOTOXIN INTERACTS WITH TUMOR NECROSIS FACTOR-α TO INDUCE VASODILATION OF ISOLATED RAT SKELETAL MUSCLE ARTERIOLES

Cited by 24 publications

References 0 publications

Dual regulation of tumor necrosis factor-α on myosin light chain phosphorylation in vascular smooth muscle

Dual regulation of tumor necrosis factor-α on myosin light chain phosphorylation in vascular smooth muscle

Increased Contractile Response to Noradrenaline Induced By Factors Associated with the Metabolic Syndrome in Cultured Small Mesenteric Arteries

Endotoxin releases a precursor to vasodilation from large veins in an NF-κB-dependent manner

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